Joe Tippens @joetippen - Twitter Profile

2 days ago

How does ivermectin combat cancer cells? Ivermectin, has shown potential anticancer effects in preclinical studies, primarily in vitro (cell cultures) and some in vivo (animal models). Its mechanisms against cancer cells are multifaceted, targeting various cellular processes. Below is a concise overview of how ivermectin may fight cancer cells, based on available research: (1) Inhibition of Cell Proliferation: -Ivermectin suppresses cancer cell growth by interfering with key signaling pathways involved in cell cycle progression, such as the Akt/mTOR, WNT-TCF, and Hippo pathways. These pathways regulate cell division and survival, and their inhibition can halt tumor growth. -It reduces the expression of pluripotency and self-renewal markers (e.g., Nanog, Oct-4, Sox-2) in cancer stem-like cells (CSCs), which are critical for tumor initiation and resistance to therapy. (2) Induction of Apoptosis (Programmed Cell Death): -Ivermectin promotes caspase-dependent apoptosis by upregulating pro-apoptotic proteins (e.g., Bax, cleaved PARP) and downregulating anti-apoptotic proteins (e.g., Bcl-2). This triggers cell death in various cancer types, including colorectal, breast, and esophageal squamous cell carcinoma (ESCC). -It induces mitochond dysfunction by inhibiting mitochond complex I, leading to reduced ATP production, increased reactive oxygen species (ROS), and oxidative stress, which damage DNA and promote apoptosis. (3) Promotion of Reactive Oxygen Species (ROS): -Ivermectin increases mitochond and total ROS levels, causing oxidative stress that damages cancer cell components (e.g., DNA, proteins). This ROS-mediated stress activates apoptosis pathways and can be reversed by antioxidants like N-acetyl-L-cysteine (NAC). (4) Induction of Immunogenic Cell Death (ICD): -Ivermectin triggers ICD, a form of cell death that stimulates an immune response. It enhances the release of ATP and HMGB1 in the tumor microenvironment, promoting inflammation and T-cell infiltration. This converts “cold” tumors (low immune activity) to “hot” tumors (high immune activity), enhancing immunotherapy efficacy (e.g., with anti-PD1 antibodies). (5) Inhibition of Multidrug Resistance (MDR): -Ivermectin inhibits P-glycoprotein (P-gp), a pump that expels chemotherapy drugs from cancer cells, causing drug resistance. By binding to the EGFR extracellular domain, it reduces EGFR activation and downstream signaling (e.g., ERK/Akt/NF-κB), lowering P-gp expression and sensitizing resistant cells to drugs like vincristine. (6) Suppression of Angiogenesis and Metastasis: -Ivermectin inhibits angiogenesis (new blood vessel formation) by targeting pathways like PAK1 and MAPK, reducing nutrient supply to tumors. It also prevents cancer cell invasion and metastasis. (7) Induction of Autophagy: -Ivermectin can induce autophagy, a process where cells degrade damaged components. In some cancers (e.g., breast), enhanced autophagy boosts anticancer effects, while in others (e.g., melanoma), it may protect cells, requiring further study to clarify its role. (8) Cell Cycle Arrest: -Ivermectin causes S-phase arrest (e.g., in colorectal cancer) or G0/G1 and subG1 accumulation (e.g., in prostate, breast, lung cancers), halting cell division and promoting cell death. Conclusion: Ivermectin fights cancer cells through multiple mechanisms, including inhibiting proliferation, inducing apoptosis, promoting ROS, triggering ICD, reversing drug resistance, and suppressing angiogenesis.

JoeTippen's tweet photo. How does ivermectin combat cancer cells?

Ivermectin, has shown potential anticancer effects in preclinical studies, primarily in vitro (cell cultures) and some in vivo (animal models). Its mechanisms against cancer cells are multifaceted, targeting various cellular processes. Below is a concise overview of how ivermectin may fight cancer cells, based on available research:

(1) Inhibition of Cell Proliferation:

-Ivermectin suppresses cancer cell growth by interfering with key signaling pathways involved in cell cycle progression, such as the Akt/mTOR, WNT-TCF, and Hippo pathways. These pathways regulate cell division and survival, and their inhibition can halt tumor growth.

-It reduces the expression of pluripotency and self-renewal markers (e.g., Nanog, Oct-4, Sox-2) in cancer stem-like cells (CSCs), which are critical for tumor initiation and resistance to therapy.

(2) Induction of Apoptosis (Programmed Cell Death):

-Ivermectin promotes caspase-dependent apoptosis by upregulating pro-apoptotic proteins (e.g., Bax, cleaved PARP) and downregulating anti-apoptotic proteins (e.g., Bcl-2). This triggers cell death in various cancer types, including colorectal, breast, and esophageal squamous cell carcinoma (ESCC).

-It induces mitochond dysfunction by inhibiting mitochond complex I, leading to reduced ATP production, increased reactive oxygen species (ROS), and oxidative stress, which damage DNA and promote apoptosis.

(3) Promotion of Reactive Oxygen Species (ROS):

-Ivermectin increases mitochond and total ROS levels, causing oxidative stress that damages cancer cell components (e.g., DNA, proteins). This ROS-mediated stress activates apoptosis pathways and can be reversed by antioxidants like N-acetyl-L-cysteine (NAC).

(4) Induction of Immunogenic Cell Death (ICD):

-Ivermectin triggers ICD, a form of cell death that stimulates an immune response. It enhances the release of ATP and HMGB1 in the tumor microenvironment, promoting inflammation and T-cell infiltration. This converts “cold” tumors (low immune activity) to “hot” tumors (high immune activity), enhancing immunotherapy efficacy (e.g., with anti-PD1 antibodies).

(5) Inhibition of Multidrug Resistance (MDR):

-Ivermectin inhibits P-glycoprotein (P-gp), a pump that expels chemotherapy drugs from cancer cells, causing drug resistance. By binding to the EGFR extracellular domain, it reduces EGFR activation and downstream signaling (e.g., ERK/Akt/NF-κB), lowering P-gp expression and sensitizing resistant cells to drugs like vincristine.

(6) Suppression of Angiogenesis and Metastasis:

-Ivermectin inhibits angiogenesis (new blood vessel formation) by targeting pathways like PAK1 and MAPK, reducing nutrient supply to tumors. It also prevents cancer cell invasion and metastasis.

(7) Induction of Autophagy:

-Ivermectin can induce autophagy, a process where cells degrade damaged components. In some cancers (e.g., breast), enhanced autophagy boosts anticancer effects, while in others (e.g., melanoma), it may protect cells, requiring further study to clarify its role.

(8) Cell Cycle Arrest:

-Ivermectin causes S-phase arrest (e.g., in colorectal cancer) or G0/G1 and subG1 accumulation (e.g., in prostate, breast, lung cancers), halting cell division and promoting cell death.

Conclusion:
Ivermectin fights cancer cells through multiple mechanisms, including inhibiting proliferation, inducing apoptosis, promoting ROS, triggering ICD, reversing drug resistance, and suppressing angiogenesis.

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